The management of common dermatological problems in older dogs (Proceedings)

To the owner, integument changes are the most obvious sign of aging. Aging of the skin and adenexa is a complex subject influenced by a combination of interrelated causative factors including wear and tear, cumulative cell damage from ionizing irradiation, and genetically preprogrammed cell changes.

The decrease in the number of active hairs and the follicular atrophy results in a thinner hair coat. Graying of the hairs especially on the muzzle is a result of the decrease in melanocyte replication. The nails become longer, malformed and more brittle. There is a progressive hyperkeratosis of the skin and hair follicles. This is especially obvious on the patient's foot pads and nose. The application of keratolytic agents or softeners is usually helpful in managing this problem. The altered sebum production and cystic dilation of the apocrine glands results in a dry, lack luster hair coat and dry skin. The dryness of the skin and coat can be helped with increased grooming, less bathing, post bathing conditioners, topical emollient (oils) and/or humectants (moisture) sprays, and essential fatty acid nutritional supplements.

Senior patients are to be more prone to food allergies, endocrine-related skin changes, pressure point calluses, adult onset Demodecosis, and cutaneous neoplasia. Sebaceous gland tumors "senile warts" account for up to 35% of all canine skin tumors but are rare in cats. They can be single but are usually multiple and occasionally ulcerate. Rarely they do they become malignant. Clinical management options include surgical excision, crysotherapy, electro surgery, laser surgery and topical chemotherapy agents including 5 FU.

Because of decreases in cellular immunity, except for fleas and ticks, infectious diseases of the skin continue to be the most common skin disease of older pets. Recurrent bacterial folliculitis, pyoderma, or otitis externa can be problematic in the older pet. The use of antiseptic shampoos, antiseptic rinses, and long term / low dose chronic antibacterial therapy is often required to manage the problem.

In older patients, Demodecosis is not usually considered in the differential diagnosis of a skin problem, but adult-onset demodex does occur and is often missed because of omitting a skin scraping in the work up. Remember demodex is a great imposer and can look like a pyoderma, an allergy, a dermatophytes infection, and even an auto-immune skin disease. The decreased cell mediated immunity may also suppress the usual inflammatory changes. With generalize adult-onset Demodecosis cases, some underlying immunosuppressive systemic disease such as Hyperadrenalcorticism, hypothyroidism, renal failure, diabetes mellitus, or neoplasia should be ruled out.

In an older dog with a late onset of pruritic skin disease, food should be strongly considered. Food allergy and food hypersensitivity are terms used to describe the immunological mediated disease reaction induced by food ingestion. Conversely food intolerance is the term used for an abnormal physiological response of foods or food additives that does not have an immunological basis. In a clinical setting, food hypersensitivity and food intolerance are rarely differentiated and refer to a non-seasonal pruritis skin disorder associated with ingestion of a substance usually found in the diet. Numerous dietary allergens exist including beef, pork, chicken, cows' milk, horsemeat, chicken egg, wheat, oats, fish, corn, and soy protein. Although any dietary protein is capable of causing pruritis, beef, dairy products, wheat and soy proteins are the most common cause of adverse cutaneous reactions. Dogs and cats can react to one or more dietary allergens.

Non-seasonal pruritis is the most common clinical sign in dogs with food-related dermatitis. In dogs the age of onset of food-related dermatitis is variable, however if the onset is in a senior dog with no previous "allergic" history, food-related allergy is much more likely that atopy. Unfortunately, the onset of food-related dermatitis is not usually associated with a recent change in diet. In one study 68% of dogs had been fed the offending diet for at least two years before onset of clinical signs. Dogs with food-related dermatitis generally will not respond as well to conventional anti-inflammatory doses of glucocorticoids, cyclosporine, antihistamine therapy, or essential fatty acid supplements as dogs with most other allergic diseases (i.e. atopy, FAD). Therefore the lack of response to these medications in a dog with mild to moderate pruritis would make Atopic dermatitis less likely than food-related dermatitis.

The primary clinical sign food-related hypersensitivities is pruritis and primary lesion is erythema. A papular eruption, urticaria, and angioedema have also been reported but are rare. Depending on the severity, as the condition progress, the secondary lesions associated with the pruritis may include alopecia, excoriations, and hyper pigmentation and lichenification with the chronic lesions. It is not uncommon for the chronic lesions to have secondary yeast infections. The distribution pattern for "food allergy" is often very similar to that seen in atopic dogs adding to the confusion. The face, ears (pinnas and external ear canals), feet, axilla, and ventral involvement are common lesion patterns. Some canine and feline patients with food related dermatitis will present with clinical tail head lesions identical to those associated with flea allergy dermatitis.

In cats, food-related dermatitis is a major cause of pruritis and self-mutilation in young to middle age cats. In cats, the pruritis tends to be localized to the head and neck. The often intense pruritis and self-trauma results in erythema, alopecia, erosions, ulcerations, and crusty lesions. Only half of the cases are considered "steroid responsive".

GI signs are present in only 10- 30% of confirmed cases. It is important to note that some of the cases of feline milliary dermatitis, esosinophilic granuloma complex, and a symmetrical alopecia caused by excessive grooming (barbering), have also been associated with food hypersensitivity.

In dogs and cats the histopathology is consistent but not helpful. The pathological diagnosis is a non-specific hypersensitivity that often includes the additional secondary pyoderma or Malassezia pathological findings. However the hypersensitivity observed could be to food, environmental allergens (atopy), contact allergens and or fleas.

Since intraderamal skin testing and serologic testing are considered marginally diagnostic, the best way to confirm a diagnosis of food-related dermatitis is evaluating the clinical response to a single novel protein test diet or a diet containing protein hydrolysates. The final confirmation is with a subsequent challenge with the patient's original diet. A single novel protein ingredient dietary trial involves feeding a diet that contains a single protein and a single carbohydrate source based on the dietary history that has not been previously fed to the patient. The single protein limited ingredient diet should be fed for at least six to eight weeks before a decision is made regarding efficacy. If no response is seen in 6 to 8 weeks, then it is unlikely that food is playing a major role in the patient's dermatitis and the diet is discontinued. However, if even a partial response is noted then the diet should be continued for an additional four weeks since some cats and dogs may take as long as 10 weeks for a maximum beneficial response. A follow up challenge with the patient's original diet is always recommended to be sure that the improvement was not coincidental with other factors. A food allergic dog or cat will typically break with pruritis and dermatitis within seven days of the challenge.

Dietary trials with protein hydrolysates are gaining favor with many veterinary dermatologists. This process of protein hydroxylation involves cleavage of protein peptide bonds into smaller units. The theory is that lower molecular weight "proteins" will not elicit an immunologically mediated response. Avoidance is the most important aspect of managing food allergies.

Superficial Necrolytic Dermatitis (SND) / Hepato-cutaneous Syndrome (HS)

Superficial Necrolytic dermatitis (SND), hepatocutaneous syndrome (HS), necrolytic migratory erythema (NME), metabolic epidermal necrosis (MEN), diabetic dermatopathy are terms used to describe a skin disease with a multi-factorial underlying etiology. This syndrome has been associated with diabetes mellitus, glucagon secreting tumors of the pancreas. However the syndrome is most often seen with a variety of canine and feline hepatopathies using the term hepatocutaneous syndrome (HS) for those conditions.

Superficial necrolytic dermatitis is generally seen in middle-aged to older dogs with the average being 10 years old. The history of skin lesions is weeks to months with a typical waxing and waning but slowly worsening course. Skin lesions are usually noted to first affect the feet and or foot pads. The lesions description includes hyperkeratosis, interdigital erythema, some erosion with crusting and occasionally intact bulla will be observed. The lesion pattern progresses to a more generalized pattern include the face, hocks, genitals, interiginous zones, lower abdomen and/or groin area. With the feet and muco-cutaneous junctions on the face the most common sites.

Skin lesions may become mildly pruritis and usually painful. Systemic signs of illness including lethargy, anorexia, and weight loss are reported in less that 20% of the cases. Laboratory changes in dogs with hepatocutaneous syndrome (HS) include increased liver enzymes especially serum alkaline phosphatase. Unfortunately many "normal" older dogs have elevated liver enzymes.

Hepatic and pancreatic ultrasonography is often helpful diagnostically. With the hepatocutaneous syndrome (HS) form of superficial necrolytic dermatitis the hepatic ultrasound generally shows a characteristic "Swiss cheese" or "honeycomb" pattern that some feel is pathognomonic for the syndrome. However in dogs with idiopathic hepatocellular collapse as the cause for their liver disease, the liver has a nodular appearance with variable sized hypoechoic regions of regeneration surrounded by an echogenic borders. There is a lack of fibrosis and reduced liver size which is seen in cirrhosis. In cases involving the glucagon secreting tumors of the pancreas, the ultrasound findings are less consistent. The pancreas and liver maybe normal or a mass may be identified in one or both organs. If a glucagonoma is suspected and ultrasonography is normal, a glucagon assay should be performed. Plasma glucagon levels are characteristically 5-10 times above the normal range.

The differential diagnosis for the cutaneous lesions is extensive however they typically have an immune mediated disease "look" and distribution pattern. However the rule outs for the hyperkeratosis lesions on the feet and face would also include zinc responsive dermatosis and generic dog food dermatosis all with a good prognosis. Initial diagnostics tests should include skin surface cytology, cytology of vesicular fluid if present. A complete blood count, a biochemical profile are indicated. Multiple skin biopsies from several affected areas are essential. It is common to find the characteristic lesions in only 1:5 biopsies submitted. With H&E staining, the epidermal parakeratotic hyperkeratosis is red, the epidermal edema as white and hyperplasic basal laver is blue. This characteristic "red, white & blue" histopathology change is pathognomonic for superficial necrolytic dermatitis. However in older lesions, this typical pattern may not be present, which may result in misdiagnosis or failure to diagnose the condition.

Numerous treatments have been used in dogs with hepatocutaneous syndrome. A 10% crystalline amino acid solution (Aminosyn, Abbott Labs) may be administered intravenously at either 25 ml/g body weight or 500 mls total volume per dog slowly over six to eight hours every 7 -10 days. The response has been variable. If minimal to no response is noted, the infusions are repeated every 7-10 days for four treatments. If an individual dog does not respond by this time, they will generally not respond. For those that respond, the amino acid infusion is repeated with each exacerbation of the skin lesions. Dogs may go several months between amino acid infusions, but some dogs will require monthly infusions to maintain remission. As the disease progresses, the need for amino acid infusions will likely increase. This solution is hypertonic and must be administered via a central vein such as the jugular vein to reduce the chance of thrombophlebitis. An oral amino acid supplementation (Promod, Ross Laboratories) has been noted to be of some benefit, perhaps because of the specific amino acid profile provided. Another choice for specific amino acids is a daily supplement of 3-6 egg yolks. The use of human body builder protein supplements has been advocated by some authors. Oral nutritional support with a high-quality protein diet such as Hill's Prescription Diet a/d or Eukanuba Recovery Formula is recommended if the dog is eating or via an enteral route. Some dogs may benefit from daily supplementation with three to six egg yolks. Zinc supplements (2 mg/kg daily of zinc methionine) and essential fatty acid supplementation (high in omega 3 fatty acids) should also be used. Temporary improvement of skin lesions and hyperkeratosis footpads may be seen with topical and systemic glucocorticoids (prednisone starting at 1 mg/kg daily). However, effects are usually transient and will eventually become refractory to these therapeutic dosages plus steroids complicate the hyperglycemia. Pain management can be an important part of the management of SND.

The prognosis with any form of Superficial Necrolytic Dermatitis is poor to grave. The mean survival time in one study was 1.6 months. The prognosis for dogs with idiopathic hepatocellular collapse is generally poor. However, there have been reported cases which have been medically managed for two to three years after diagnosis of the disease.